View source for Norepinephrine

{{chembox
|   ImageFile = Norepinephrine structure with descriptor.svg
|   ImageSize = 180px
|   ImageFile1 = Norepinephrine-3d-CPK.png
|   ImageSize1 = 180px
|   Name = Norepinephrine
|   Reference =<ref>''Merck Index'', 11th Edition, '''6612'''.</ref>
|   IUPACName = 4-[(1''R'')-2-amino-1-hydroxyethyl]benzene-1,2-diol
|   OtherNames = Noradrenaline<br />(''R'')-(–)-Norepinephrine
| Section1 = {{Chembox Identifiers
| CASNo =  51-41-2 (l)
|   CASOther =  [http://www.commonchemistry.org/ChemicalDetail.aspx?ref=138-65-8 138-65-8](dl)
|   ChemSpiderID = 388394
  }}
| Section2 = {{Chembox Properties
|   Formula = |C=8|H=11|N=1|O=3
|   MolarMass = 169.18 g/mol
|   MeltingPt = L: 216.5–218 °C (''decomp.'')<br />D/L: 191 °C (''decomp.'')
  }}
}}

'''Norepinephrine''' ([[International Nonproprietary Name|INN]]) (abbreviated '''norepi''' or '''NE''') 
or '''noradrenaline''' ([[British Approved Name|BAN]]) (abbreviated '''NA''' or '''NAd''') is a [[catecholamine]] with multiple roles including as a [[hormone]] and a [[neurotransmitter]].<ref>
{{cite web
|url=http://dictionary.reference.com/browse/Norepinephrine
|title=Norepinephrine definition | Dictionary.com
|publisher=dictionary.reference.com
|accessdate=2008-11-24
|last=
|first=
}}
</ref>

As a [[stress hormone]], norepinephrine affects parts of the brain where [[attention]] and responding actions are controlled. Along with [[epinephrine]], norepinephrine also underlies the [[fight-or-flight response]], directly increasing [[heart rate]], triggering the release of [[glucose]] from energy stores, and increasing blood flow to [[skeletal muscle]]. Norepinephrine can also suppress [[inflammation|neuroinflammation]] when released diffusely in the brain from the [[locus ceruleus]].<ref name="Heneka2010">Heneka MT, Nadrigny F, Regen T, Martinez-Hernandez A, Dumitrescu-Ozimek L, Terwel D, Jardanhazi-Kurutz D, Walter J, Kirchhoff F, Hanisch UK, Kummer MP. (2010). [http://www.pnas.org.libproxy.ucl.ac.uk/content/107/13/6058.full.pdf Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine.] Proc Natl Acad Sci U S A. 107:6058–6063  {{doi|10.1073/pnas.0909586107}} PMID 20231476</ref> 

When norepinephrine acts as a [[drug]] it increases [[blood pressure]] by increasing vascular tone through [[adrenergic receptor|α-adrenergic receptor]] activation. The resulting increase in vascular resistance triggers a compensatory [[reflex]] that overcomes its direct stimulatory effects on the heart, called the [[baroreceptor reflex]], which results in a drop in heart rate called [[reflex bradycardia]]. 

Norepinephrine is synthesized from [[dopamine]] by [[dopamine β-hydroxylase]].<ref>{{cite web |title=Introduction to Autonomic Pharmacology |url=http://www.fleshandbones.com/readingroom/pdf/225.pdf |format=PDF|publisher=Elsevier International}}&nbsp;Link redirected to commercial site!</ref> It is released from the [[adrenal medulla]] into the blood as a [[hormone]], and is also a [[neurotransmitter]] in the [[central nervous system]] and [[sympathetic nervous system]] where it is released from noradrenergic [[neuron]]s. The actions of norepinephrine are carried out via the binding to [[adrenergic receptor]]s.

==Etymology==
The term "norepinephrine" is derived from the chemical prefix ''[[nor-]]'', which indicates that norepinephrine is the next lower [[homology (chemistry)|homolog]] of [[epinephrine]]. The two structures differ only in that epinephrine has a methyl group attached to its nitrogen, while the methyl group is replaced by a hydrogen atom in norepinephrine.

==Chemistry==
Norepinephrine is a [[catecholamine]] and a [[phenethylamine]]. The natural [[stereoisomer]] is <small>L</small>-(−)-(''R'')-norepinephrine. The prefix ''[[nor-]]'', is derived from the German abbreviation for ''"N ohne Radikal"'' (N, the symbol for nitrogen, without [[radical (chemistry)|radical]]),<ref name="nor">[http://www.drugsinfo.net/tihkal/tihkal01.html TIHKAL on "nor"]</ref> referring to the absence of the [[methyl]] [[functional group]] at the nitrogen atom.

==Origins==
Norepinephrine is released when a host of [[physiology|physiological]] changes are activated by a stressful event.

In the brain, this is caused in part by activation of an area of the [[brain stem]] called the [[locus ceruleus]]. This nucleus is the origin of most norepinephrine pathways in the brain. Noradrenergic neurons project bilaterally (send signals to both sides of the brain) from the locus ceruleus along distinct pathways to many locations, including the [[cerebral cortex]], [[limbic system]], and the [[spinal cord]], forming a [[neurotransmitter system]].

Norepinephrine is also released from [[postganglionic neuron]]s of the [[sympathetic nervous system]], to transmit the [[fight-or-flight]] response in each tissue respectively. The [[adrenal medulla]] can also be counted to such postganglionic nerve cells, although they release norepinephrine into the blood.

===Norepinephrine system===
The noradrenergic neurons in the brain form a [[neurotransmitter system]], that, when activated, exerts effects on large areas of the brain. The effects are alertness and [[arousal]], and influences on the [[reward system]].

Anatomically, the noradrenergic neurons originate both in the [[locus coeruleus]] and the [[lateral tegmental field]]. The axons of the neurons in the [[locus coeruleus]] act on [[adrenergic receptors]] in:

* [[Amygdala]]
* [[Cingulate gyrus]]
* [[Cingulum]]
* [[Hippocampus]]
* [[Hypothalamus]]
* [[Neocortex]]
* [[Spinal cord]]
* [[Striatum]]
* [[Thalamus]]

On the other hand, axons of neurons of the [[lateral tegmental field]] act on [[adrenergic receptor]]s in [[hypothalamus]], for example.

This structure explains some of the clinical uses of norepinephrine, since a modification of the system affects large areas of the brain.

==Mechanism==
Norepinephrine is synthesized from [[tyrosine]] as a precursor, and packed into synaptic vesicles. It performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells.

===Biosynthesis===

Norepinephrine is synthesized by a series of enzymatic steps in the [[adrenal medulla]] and [[postganglionic neuron]]s of the [[sympathetic nervous system]] from the [[amino acid]] [[tyrosine]]:

* The first reaction is the [[hydroxylation]] into [[L-DOPA|dihydroxyphenylalanine (L-DOPA)]] (DOPA = 3,4-DiHydroxy-L-Phenylalanine), catalyzed by [[tyrosine hydroxylase]]. This is the rate-limiting step.
* This is followed by [[decarboxylation]] into the [[neurotransmitter]] [[dopamine]], catalyzed by [[pyridoxal phosphate]] & [[DOPA decarboxylase]].
* Last is the final β-[[oxidation]] into norepinephrine by [[dopamine beta hydroxylase]], requiring [[ascorbate]] as a cofactor (electron donor).

<gallery>
Image:L-tyrosine-skeletal.png|[[Tyrosine]]
Image:3,4-Dihydroxy-L-phenylalanin (Levodopa).svg|[[Levodopa]]
Image:Dopamine2.svg|[[Dopamine]]
Image:Norepinephrine_structure_with_descriptor.svg|Norepinephrine
</gallery>

===Vesicular transport===
Between the decarboxylation and the final β-oxidation, norepinephrine is transported into [[synaptic vesicle]]s. This is accomplished by [[vesicular monoamine transporter]] (VMAT) in the [[lipid bilayer]]. This transporter has equal affinity for norepinephrine, [[epinephrine]] and [[isoprenaline]].<ref name=Rang167> {{cite book |author=Rang, H. P. |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |pages= |isbn=0-443-07145-4 |oclc= |doi = }} Page 167</ref>

===Release===
To perform its functions, norepinephrine needs to be released from synaptic vesicles. Many substances modulate this release, some inhibiting it and some stimulating it.

For instance, there are inhibitory [[α2 adrenergic receptor]]s presynaptically, that gives [[negative feedback]] on release by [[homotropic modulation]].

===Receptor binding===
{{Main|Adrenergic receptor}}

Norepinephrine performs its actions on the target cell by binding to and activating [[adrenergic receptor]]s. The target cell expression of different types of receptors determines the ultimate cellular effect, and thus norepinephrine has different actions on different [[cell type]]s.

===Termination===
Signal termination is a result of reuptake and degradation.

====Uptake====
Extracellular uptake of norepinephrine into the cytosol is either done presynaptically (uptake 1) or by non-neuronal cells in the vicinity (uptake 2). Furthermore, there is a ''vesicular uptake'' mechanism from the cytosol into [[synaptic vesicles]].

{| class="wikitable"
|+Comparison of norepinephrine uptake
! Uptake
! Transporter
![[Michaelis–Menten kinetics|V<sub>max</sub>]] ([[nano|n]][[mol]]/g/min)<ref name=Rang167rat> These values are from rat heart. Unless else specified in table, then ref is: {{cite book |author=Rang, H. P. |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |pages= |isbn=0-443-07145-4 |oclc= |doi = }} Page 167</ref>
![[Michaelis constant|K<sub>M</sub>]]<ref name=Rang167rat/>
!Specificity<ref name=Rang167unless> Unless else specified in table, then ref is: {{cite book |author=Rang, H. P. |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |pages= |isbn=0-443-07145-4 |oclc= |doi = }} Page 167</ref>
!Location
!Other substrates<ref name=Rang167unless/>
!Inhibitors <ref name=Rang&Dale6th>Unless else specified in boxes, then ref is: {{cite book |author=Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. |title=Rang & Dale's pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2007 |pages= |isbn=0-443-06911-5 |oclc= |doi= |accessdate=}}</ref>
|-
!Uptake 1
| [[Norepinephrine transporter]]<ref name=Rang&Dale6th/> || 1.2 || 0.3 || norepinephrine > [[epinephrine]] > [[isoprenaline]] || presynaptic ||
*[[methylnoradrenaline]] (nasal [[decongestant]])
*[[tyramine]]
*[[guanethidine]]
|
*[[Cocaine]]
*[[Tricyclic antidepressant]]s (e.g. [[desipramine]])
*[[Phenoxybenzamine]]
*[[Amphetamine]]
|-
!Uptake 2
|  || 100 || 250 || [[epinephrine]] > norepinephrine > [[isoprenaline]] || [[cell membrane]] of non-[[neuronal]] cells<ref name=Rang167/>
|
*[[dopamine]]
*[[5-HT]]
*[[histamine]]
|
*[[normetanephrine]]
*[[steroid hormone]]s (e.g. [[corticosterone]])
*[[phenoxybenzamine]]
|-
! Vesicular
| [[Vesicular monoamine transporter|VMAT]]<ref name=Rang&Dale6th/>
| -<ref name=Rang&Dale6th/>
| ~0.2<ref name=Rang&Dale6th/>
| norepinephrine > epinephrine > isoprenaline<ref name=Rang&Dale6th/>
| [[Synaptic vesicle]] membrane<ref name=Rang&Dale6th/>
| 
*dopamine<ref name=Rang&Dale6th/>
*5-HT<ref name=Rang&Dale6th/>
*guanethidine<ref name=Rang&Dale6th/>
*[[MPP+]]<ref name=Rang&Dale6th/>
|
*[[Reserpine]]<ref name=Rang&Dale6th/>
*[[Tetrabenazine]]
|}

====Degradation====
[[File:Noradrenaline breakdown.svg|thumb|350px|Norepinephrine degradation. Enzymes are shown in boxes. <ref name=Rang&Dale6th-11-4>Figure 11-4 in: {{cite book |author=Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. |title=Rang & Dale's pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2007 |pages= |isbn=0-443-06911-5 |oclc= |doi= |accessdate=}}</ref>]]
In mammals, norepinephrine is rapidly degraded to various [[metabolite]]s. The principal metabolites are:

* [[Normetanephrine]] (via the enzyme catechol-O-methyl transferase, [[catechol-O-methyl transferase|COMT]])
* [[3,4-Dihydroxymandelic acid]] (via monoamine oxidase, [[MAO-A|MAO]])
* [[Vanillylmandelic acid]] (3-Methoxy-4-hydroxymandelic acid), also referred to as vanilmandelate or VMA (via [[MAO-A|MAO]])
* [[3-Methoxy-4-hydroxyphenylethylene glycol]], "MHPG" or "MOPEG" (via [[MAO-A|MAO]])
* [[Epinephrine]] (via [[Phenylethanolamine N-methyltransferase|PNMT]])<ref>"Endokrynologia Kliniczna" ISBN 83-200-0815-8, page 502</ref>

In the periphery, VMA is the major metabolite of catecholamines, and is excreted unconjugated in the urine. A minor metabolite (although the major one in the central nervous sytem) is MHPG, which is partly conjugated to sulfate or glucuronide derivatives and excreted in the urine.<ref name=Rang&Dale6th-11>Chapter 11 in: {{cite book |author=Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. |title=Rang & Dale's pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2007 |pages= |isbn=0-443-06911-5 |oclc= |doi= |accessdate=}}</ref>

==Noradrenergic agents==
===By indication===
Norepinephrine may be used for the indications attention-deficit/hyperactivity disorder, depression and hypotension. Norepinephrine, as with other catecholamines, itself cannot cross the blood-brain barrier, so drugs such as amphetamines are necessary to increase brain levels.

====Attention-deficit/hyperactivity disorder====
<!-- heading: "Function in the brain: attention" used to create a synergy with the Dopamine article (September 2006) -->
Norepinephrine, along with [[dopamine]], has come to be recognized as playing a large role in attention and focus. For people with [[ADHD]], psychostimulant medications such as [[methylphenidate]] (Ritalin/Concerta), [[dextroamphetamine]] (Dexedrine), and [[Adderall]] (a mixture of dextroamphetamine and [[racemic]] [[amphetamine]] salts) are prescribed to help increase levels of norepinephrine and dopamine. [[Atomoxetine]] (Strattera) is a [[selective norepinephrine reuptake inhibitor]], and is a unique ADHD medication, as it affects only norepinephrine, rather than dopamine. As a result, Strattera has a lower abuse potential. However, it may not be as effective as the psychostimulants are with many people who have ADHD. Consulting with a physician, physician assistant or [[nurse practitioner]] is needed to find the appropriate medication and dosage. (Other SNRIs, currently approved as antidepressants, have also been used [[off-label]] for treatment of ADHD.)

====Depression====
{{main|Major depressive disorder}}
Differences in the norepinephrine system are implicated in [[clinical depression|depression]]. [[Serotonin-norepinephrine reuptake inhibitor]]s are [[antidepressants]] that treat depression by increasing the amount of [[serotonin]] and norepinephrine available to [[postsynaptic]] cells in the brain. There is some recent evidence implying that [[SNRI]]s may also increase [[dopamine]] transmission.<ref>http://stahlonline.cambridge.org/prescribers_drug.jsf?page=0521683505c95_p539-544.html.therapeutics&name=Venlafaxine&title=Therapeutics</ref> This is because [[SNRI]]s work by inhibiting reuptake, i.e. preventing the [[serotonin]] and norepinephrine transporters from taking their respective [[neurotransmitter]]s back to their storage [[Synaptic vesicle|vesicles]] for later use. If the [[norepinephrine transporter]] normally recycles some [[dopamine]] too, then [[SNRI]]s will also enhance [[dopaminergic]] transmission. Therefore, the [[antidepressant]] effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in [[dopamine]] (particularly in the [[prefrontal cortex]] of the brain).

[[Tricyclic antidepressant]]s (TCAs) increase '''norepinephrine''' activity as well. Most of them also increase [[serotonin]] activity, but tend to produce unwanted side effects due to the nonspecific inactivation of [[histamine]], [[acetylcholine]] and [[alpha-1 adrenergic receptor|alpha-1 adrenergic]] receptors. Common side effects include sedation, dry mouth, constipation, sinus tachycardia, memory impairment, orthostatic hypotension, blurred vision and weight gain.<ref>http://www.preskorn.com/columns/9803.html</ref> For this reason, they have largely been replaced by newer selective reuptake drugs.  These include the [[Selective serotonin reuptake inhibitor|SSRI]]s, e.g. [[fluoxetine]] (Prozac), which however have little or no effect on norepinephrine, and the newer [[SNRI]]s described above, such as [[venlafaxine]] (Effexor) and [[duloxetine]] (Cymbalta).

====Hypotension====
Norepinephrine is also used as a [[vasopressor]] medication (for example, brand name Levophed) for patients with critical [[hypotension]]. It is given intravenously and acts on both α<sub>1</sub> and α<sub>2</sub> adrenergic receptors to cause vasoconstriction. Its effects are often limited to the increasing of blood pressure through agonist activity on α<sub>1</sub> and α<sub>2</sub> receptors and causing a resultant increase in [[peripheral vascular resistance]]. At high doses, and especially when it is combined with other vasopressors, it can lead to limb [[ischemia]] and limb death. Norepinephrine is mainly used to treat patients in vasodilatory shock states such as [[septic shock]] and [[neurogenic shock]] and has shown a survival benefit over [[dopamine]].

===By site of action===
Different [[medication]]s affecting norepinephrine function have their targets at different points in the mechanism, from synthesis to signal termination.

====Synthesis modulators====
[[α-methyltyrosine]] is a substance that intervenes in norepinephrine synthesis by substituting tyrosine for [[tyrosine hydroxylase]], and blocking this enzyme.

====Vesicular transport modulators====
This transportation can be inhibited by [[reserpine]] and [[tetrabenazine]].<ref name=Rang167/>

====Release modulators====
{| class="wikitable sortable"
|+Inhibitors of norepinephrine release
|-
!Substance<ref name=Rang129> Unless else specified in table, then ref is: {{cite book |author=Rang, H. P. |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |pages= |isbn=0-443-07145-4 |oclc= |doi = }} Page 129</ref>
!Receptor<ref name=Rang129/>
|-
| [[acetylcholine]] || [[muscarinic receptor]]
|-
| ''norepinephrine'' (itself)/[[epinephrine]] || [[α2 receptor]]
|-
| [[5-HT]] || [[5-HT receptor]]
|-
| [[adenosine]] || [[P1 receptor]]
|-
| [[prostaglandin E|PGE]] || [[EP receptor]]
|-
| [[histamine]] || [[H2 receptor]]
|-
| [[enkephalin]] || [[delta Opioid receptor|δ receptor]]
|-
| [[dopamine]] || [[D2 receptor]]
|-
| [[adenosine triphosphate|ATP]] || [[P2 receptor]]
|}

{| class="wikitable sortable"
|+Stimulators of norepinephrine release
|-
!Substance<ref name=Rang129/>
!Receptor<ref name=Rang129/>
|-
| [[adrenaline]] || [[β2 receptor]]
|-
| [[angiotensin II]] || [[AT1 receptor]]
|-
|}

====Receptor binding modulators====
Examples include [[alpha blockers]] for the α-receptors, and [[beta blocker]]s for the β-receptors.

====Termination modulators====
=====Uptake modulators=====
Inhibitors<ref name=Rang167/> of uptake 1 include:
*[[cocaine]]
*[[tricyclic antidepressant]]s
**[[desipramine]]
*[[phenoxybenzamine]]
*[[amphetamine]]

Inhibitors<ref name=Rang167/> of uptake 2 include:
*[[normetanephrine]]
*[[steroid hormone]]s
*[[phenoxybenzamine]]


====Anti-Inflammatory agent role in Alzheimer’s Disease====

The norepinephrine from locus ceruleus cells in addition to its neurotransmitter role locally defuses from "varicosities". As such it provides an endogenous [[anti-inflammatory]] agent in the microenvironment around the neurons, [[glial cell]]s, and blood vessels in the neocortex and hippocampus.<ref name="Heneka2010">Heneka MT, Nadrigny F, Regen T, Martinez-Hernandez A, Dumitrescu-Ozimek L, Terwel D, Jardanhazi-Kurutz D, Walter J, Kirchhoff F, Hanisch UK, Kummer MP. (2010). [http://www.pnas.org.libproxy.ucl.ac.uk/content/107/13/6058.full.pdf Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine.] Proc Natl Acad Sci U S A. 107:6058–6063  {{doi|10.1073/pnas.0909586107}} PMID 20231476</ref> Up to 70% of norepinephrine projecting cells are lost in [[Alzheimer’s Disease]]. It has been shown that norepinephrine stimulates mouse microglia to suppress [[Aβ]]-induced production of [[cytokine]]s and their [[phagocytosis]] of Aβ suggesting this loss might have a role in causing this disease.<ref name="Heneka2010"/>

==Nutritional sources==
[[Image:L-Tyrosin - L-Tyrosine.svg|thumb|right|Shown here is the chemical structure of [[tyrosine]]. The [[biosynthesis]] of norepinephrine depends upon the presence of [[tyrosine]], an amino acid building block of many proteins in meat, nuts and eggs, for example.]]

The synthesis of norepinephrine depends on the presence of [[tyrosine]], an amino acid found in proteins such as meat, nuts, and eggs. Dairy products such as cheese also contain high amounts of tyrosine (the amino acid is named for "tyros," the Greek word for cheese). Tyrosine is the precursor to [[dopamine]], which is in itself a precursor of epinephrine and norepinephrine.

[[Serotonin]], a neurotransmitter that is in many ways the opposite of the [[catecholamine]]s, is also directly synthesized from an amino acid ([[tryptophan]]). However, tryptophan has a somewhat different process of degradation. When serotonin is catabolized in the body, it does not break down into useful substrates in the way that dopamine is further degraded into [[epinephrine]] and norepinephrine. Instead, it breaks down into 5-hydroxyindoleacetic acid (5-HIA), an organic acid which may be harmful in high amounts. Tryptophan can further be catabolized into [[kynurenate]], [[quinolinate]], and [[picolinate]], harmful substances that are generally regarded as markers of bodily inflammation.

[[Banana]] peels contain significant amounts of norepinephrine and [[dopamine]].<ref name=ahpg >{{cite journal
  | last = Kanazawa
  | first = Kazuki
  | authorlink =
  | coauthors = Hiroyuki Sakakibara
  | title = High content of Dopamine, a strong antioxidant, in Cavendish banana
  | journal = Journal of Agriculture and Food Chemistry
  | volume = 48
  | issue =
  | pages = 844–848
  | publisher =
  | location =
  | year = 2000
  | url = http://152.1.118.33/Files/Journal%20of%20Agricultural%20and%20Food%20Chemistry%202000%2048%20(3)%20844-848.pdf
  |format=PDF| doi =10.1021/jf9909860
  | id =
  | accessdate = 8 November 2007 }}</ref>

==See also==
*[[Norepinephrine bitartrate]]
*[[Catecholaminergic polymorphic ventricular tachycardia]]

==External links==
* [http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec2_1.html Mental Health: A report of surgeon general. Etiology of Anxiety Disorders]
* http://www.biopsychiatry.com/nordop.htm

==References==
{{More footnotes|date=May 2008}}
{{Citation style|date=September 2007}}
{{Reflist|2}}

{{Phenethylamines}}
{{Hormones}}
{{Amino alcohols}}
{{Adrenergic and dopaminergic agents}}
{{Adrenergics}}
{{Neurotransmitters}}

[[Category:Cardiac stimulants]]
[[Category:Catecholamines]]
[[Category:Hormones of the suprarenal medulla]]
[[Category:Neurotransmitters]]

[[ar:نورإبينفرين]]
[[bg:Норадреналин]]
[[ca:Noradrenalina]]
[[cs:Noradrenalin]]
[[da:Noradrenalin]]
[[de:Noradrenalin]]
[[dv:ނޯއެޑްރެނަލިން]]
[[et:Noradrenaliin]]
[[es:Noradrenalina]]
[[eo:Noradrenalino]]
[[fa:نوراپی‌نفرین]]
[[fr:Noradrénaline]]
[[hr:Noradrenalin]]
[[it:Noradrenalina]]
[[he:נוראדרנלין]]
[[la:Noradrenalinum]]
[[lt:Noradrenalinas]]
[[hu:Noradrenalin]]
[[mk:Норадреналин]]
[[nl:Noradrenaline]]
[[ja:ノルアドレナリン]]
[[no:Noradrenalin]]
[[pl:Noradrenalina]]
[[pt:Noradrenalina]]
[[ru:Норадреналин]]
[[sq:Noradrenalina]]
[[sl:Noradrenalin]]
[[sr:Норадреналин]]
[[fi:Noradrenaliini]]
[[sv:Noradrenalin]]
[[tr:Noradrenalin]]
[[uk:Норадреналін]]
[[zh:去甲肾上腺素]]
[[Category:2Fix]]